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Wnt/Beta-catenin/Esrrb signalling controls the tissue-scale reorganization and maintenance of the pluripotent lineage during murine embryonic diapause

Author

Listed:
  • Rui Fan

    (Max Planck Institute for Molecular Biomedicine)

  • Yung Su Kim

    (Max Planck Institute for Molecular Biomedicine)

  • Jie Wu

    (Department of Chemistry and Biochemistry)

  • Rui Chen

    (Max Planck Institute for Molecular Biomedicine)

  • Dagmar Zeuschner

    (Max Planck Institute for Molecular Biomedicine)

  • Karina Mildner

    (Max Planck Institute for Molecular Biomedicine)

  • Kenjiro Adachi

    (Max Planck Institute for Molecular Biomedicine)

  • Guangming Wu

    (Max Planck Institute for Molecular Biomedicine
    Guangzhou Regenerative Medicine and Health Guangdong Laboratory)

  • Styliani Galatidou

    (Max Planck Institute for Molecular Biomedicine)

  • Jianhua Li

    (Max Planck Institute for Molecular Biomedicine)

  • Hans R. Schöler

    (Max Planck Institute for Molecular Biomedicine)

  • Sebastian A. Leidel

    (Department of Chemistry and Biochemistry)

  • Ivan Bedzhov

    (Max Planck Institute for Molecular Biomedicine)

Abstract

The epiblast, which provides the foundation of the future body, is actively reshaped during early embryogenesis, but the reshaping mechanisms are poorly understood. Here, using a 3D in vitro model of early epiblast development, we identify the canonical Wnt/β-catenin pathway and its central downstream factor Esrrb as the key signalling cascade regulating the tissue-scale organization of the murine pluripotent lineage. Although in vivo the Wnt/β-catenin/Esrrb circuit is dispensable for embryonic development before implantation, autocrine Wnt activity controls the morphogenesis and long-term maintenance of the epiblast when development is put on hold during diapause. During this phase, the progressive changes in the epiblast architecture and Wnt signalling response show that diapause is not a stasis but instead is a dynamic process with underlying mechanisms that can appear redundant during transient embryogenesis.

Suggested Citation

  • Rui Fan & Yung Su Kim & Jie Wu & Rui Chen & Dagmar Zeuschner & Karina Mildner & Kenjiro Adachi & Guangming Wu & Styliani Galatidou & Jianhua Li & Hans R. Schöler & Sebastian A. Leidel & Ivan Bedzhov, 2020. "Wnt/Beta-catenin/Esrrb signalling controls the tissue-scale reorganization and maintenance of the pluripotent lineage during murine embryonic diapause," Nature Communications, Nature, vol. 11(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19353-0
    DOI: 10.1038/s41467-020-19353-0
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    Cited by:

    1. Binyamin Duethorn & Fabian Groll & Bettina Rieger & Hannes C. A. Drexler & Heike Brinkmann & Ludmila Kremer & Martin Stehling & Marie-Theres Borowski & Karina Mildner & Dagmar Zeuschner & Magdalena Ze, 2022. "Lima1 mediates the pluripotency control of membrane dynamics and cellular metabolism," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    2. Sina Schumacher & Max Fernkorn & Michelle Marten & Rui Chen & Yung Su Kim & Ivan Bedzhov & Christian Schröter, 2024. "Tissue-intrinsic beta-catenin signals antagonize Nodal-driven anterior visceral endoderm differentiation," Nature Communications, Nature, vol. 15(1), pages 1-15, December.
    3. Paraskevi Athanasouli & Martina Balli & Anchel Jaime-Soguero & Annekatrien Boel & Sofia Papanikolaou & Bernard K. Veer & Adrian Janiszewski & Tijs Vanhessche & Annick Francis & Youssef El Laithy & Ant, 2023. "The Wnt/TCF7L1 transcriptional repressor axis drives primitive endoderm formation by antagonizing naive and formative pluripotency," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    4. Timo N. Kohler & Joachim Jonghe & Anna L. Ellermann & Ayaka Yanagida & Michael Herger & Erin M. Slatery & Antonia Weberling & Clara Munger & Katrin Fischer & Carla Mulas & Alex Winkel & Connor Ross & , 2023. "Plakoglobin is a mechanoresponsive regulator of naive pluripotency," Nature Communications, Nature, vol. 14(1), pages 1-19, December.

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